Implication of the chemokine CCL2 in trigeminal nociception and traumatic neuropathic orofacial pain.

摘要: Background Chemokine (C-C motif) ligand 2 (CCL2) participates in different mechanisms contributing to the spinal cord inflammation and pain development after sciatic nerve injury. Recent data also support its role orofacial thermal hypersensitivity, although implication phases of trigeminal emergence is unclear. We assessed importance CCL2 signalling biochemical behavioural alterations during early late stages following chronic constriction injury infraorbital (ION-CCI), a model peripheral traumatic pain. Methods After evaluating consequences intracisternal injection naive rats, we determined expression changes for CCL2, inflammatory glia activation markers somatosensory complex (STC) ganglia (TG) ION-CCI. The was using pre-emptive or ‘curative’ treatment with specific receptor antagonist – INCB3344. Results Exogenous evoked spontaneous behaviour reminiscent marked mechanical associated increased proinflammatory cytokines glial STC TG. CCL2-evoked were prevented by co-administration INCB3344. Two weeks ION-CCI, mRNA up-regulated, CCL2-immunoreactivity accumulated central ganglionic tissues. At this time, repeated administration INCB3344 did not attenuate ION-CCI-associated nor changes. By contrast, delayed allodynia alterations. Conclusions Our suggest that involved principally events accompanying ION lesion rather than long-term maintenance hypersensitivity.